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J. Virol. doi:10.1128/JVI.00403-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

EPSTEIN-BARR VIRUS INDUCES MCP-1 SECRETION BY HUMAN MONOCYTES VIA TLR2

Viral Immunology Laboratory, CHUL Research Center (CHUQ) and Université Laval, Québec, QC, Canada G1V-4G2; Centre for the Study of Host Resistance and the Research Institute of the McGill University Health Centre, Departments of Medicine and Microbiology & Immunology, McGill University, Montréal, QC, Canada H3A 2B4

^* To whom correspondence should be addressed. Email: jean.gosselin{at}crchul.ulaval.ca.

	Abstract

Epstein-Barr virus (EBV) is a gamma herpesvirus infecting the majority of worldwide adult population. TLR2, a member of the Toll-like receptor family, has been implicated in the immune response to different viruses including members of the herpesvirus family such as human cytomegalovirus, herpes simplex-1 and varicella zoster virus. In this report, we demonstrate that infectious and U.V.-inactivated EBV virions lead to the activation of NF-B through TLR2 using HEK293 cells co-transfected with TLR2 expressing vector along with NF-B-Luc reporter plasmid. NF-B activation in HEK293-TLR2 cells by EBV was not enhanced by the presence of CD14. Effect of EBV was abrogated by pre-treating HEK293-TLR2 cells with blocking anti-TLR2 antibodies or by pre-incubating viral particles with neutralizing anti-EBV antibodies 72A1. In addition, EBV infection of primary human monocytes induced the release of monocyte-chemotactic protein-1 (MCP-1), and the use of small-interfering RNA targeting TLR2 significantly reduced such a chemokine response to EBV. Taken together, these results indicate that TLR2 may be an important pattern recognition receptor in the immune response directed against EBV infection.

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